The statements in this section merely provide background information related to the present disclosure and may not constitute prior art.
Medical research has demonstrated a significant source of systemic disease is related to specific oral bacteria, with special emphasis on certain gram negative anaerobic bacteria that have been found associated with a variety of systemic inflammatory responses and appear to originate only in periodontal pockets and enter the bloodstream through a close proximity to the host circulatory system. There are very few regions of the body which can readily be rendered conducive to the growth of anaerobic bacteria. Deeper periodontal pockets are one region that readily demonstrates infections that are predominantly anaerobic, with gram-negative bacteria being the most common isolates. The anatomic closeness of these biofilm periopathogens to the bloodstream can facilitate bacteremia and systemic spread of bacterial products, components, and immunocomplexes (antigen/antibody reactions, chemokines and cytokines).
It has been found that these oral periopathogens can become systemic. Research has demonstrated that bacteremia was observed in 100% of the patients after dental extraction and in 70% after dental scaling. Mastication on infected gum tissues increases systemic bacterial endotoxins levels four-fold. Simple oral hygiene procedures, such as brushing of the teeth, can increase the prevalence of bacteremia from 17 to 40%. Research has also demonstrated that the dissemination of oral microorganisms into the bloodstream is common. In fact, it has been found that within less than 1 minute after an oral procedure, organisms from an infected site can reach the heart, lungs, and peripheral blood capillary system of a patient. These periopathogens can cause host injury (exotoxins and toxic bacterial products), inflammation (immune system—antigen/antibody reactions) and infections (bacteremia) in a person. Periodontitis may affect the host's susceptibility to systemic disease in three ways: by shared risk factors, by subgingival biofilms acting as reservoirs of bacteria, and through the periodontium acting as a reservoir of inflammatory mediators.
It has also been found that controlling these periopathogens in the mouth decreases systemic responses. Studies have evaluated periodontitis and C-reactive protein (CRP) levels in patients. For example, one study evaluated three groups: (1) an untreated control group of 24 subjects; (2) a group of 21 subjects with a standard regimen of periodontal therapy (SPT), consisting of subgingival mechanical instrumentation; and (3) a group of 20 subjects who had an intensive course of periodontal treatment (IPT), consisting of SPT with adjunctive local delivery of minocycline-HCl (Arestin®, Orapharma, Warminster, Pa., USA). The results of this study in both treatment groups identified a considerable reduction of periodontal lesions after therapy [60±27 (P<0.0001, N=21) and 60±23 (P<0.0001, N=20) mean differences tested by t test, respectively]. No changes were observed in the untreated controls. Similar results were found in the IL-6 markers. The report of that study concluded that periodontitis causes moderate systemic inflammation in systemically healthy patients because reducing the periodontal disease resulted in a reduction in the systemic inflammatory markers.
Periodontitis is an infection that can stimulate the liver to produce C-reactive protein (CRP) (a marker of inflammation), which in turn will form deposits on injured blood vessels. CRP binds to cells that are damaged and fixes complement, which activates phagocytes, including neutrophils. These cells release nitric oxide, thereby contributing to atheroma formation. It has been found that patients with adult periodontitis have higher levels of CRP and haptoglobin than subjects without periodontitis. Both CRP and haptoglobin levels decline significantly after periodontal therapy. Additionally, in another study of 153 systemically healthy subjects consisting of 108 untreated periodontitis patients and 45 control subjects, the mean plasma CRP levels were higher in the periodontitis patients. Patients with severe periodontitis had significantly higher CRP levels than mild-periodontitis patients, and both had significantly higher levels than the controls. Another recent study evaluated the relationship of cardiovascular disease and CRP into three groups of adults: i) had neither periodontal nor cardiovascular disease, ii) had only one of these two diseases, and iii) had both of two diseases. In those with both heart disease and periodontal disease, the mean level of CRP (8.7 g/ml) was significantly different from that (1.14 g/ml) in controls with neither disease. It was also shown in that study that treatment of the periodontal disease caused a 65% reduction in the level of CRP within 3 months of treatment.
However, current methods to treat periodontal disease and the resulting effects thereof suffer from a number of significant drawbacks and are often ineffective in addressing the systemic effects of periodontal originated disease. Many of the systemic biomarkers decrease following conventional oral disinfection, but these biomarker decreases are short lived and return to abnormal elevated pre-treatment levels. The inventor of the present methods and systems has identified a significant need and desired benefit to many patients in developing new procedures and systems that address the systemic effects of periodontal originated diseases.